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SEMA3F-deficient colorectal cancer cells promote lymphangiogenesis: fatty acid metabolism replace glycolysis for energy supply during lymphatic endothelial cells …

biorxiv. 2019; 
Xiaoyuan Fu, Miaomiao Tao, Hongbo Ma, Cancan Wang, Yanyan Li, Xiaoqiao Hu, Xiurong Qin, Renming Lv, Gengdou Zhou, Jun Wang, Meiyu Zhou, Guofa Xu, Zexin Wang, Min Chen, Qi Zhou
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Gene Synthesis To stimulate the biogenesis of mitochondria, cells were pretreated with interleukin 4 (IL-4) (Cat. # Z02925-10, GenScript) at a concentration of 5 ng/ml for 24h. Get A Quote

摘要

lymphangiogenesis as a process is colorectal cancer first metastasis via lymphatic vessels to proximal lymph nodes. The fuel metabolism in mitochondrial and support proliferation of lymphatic endothelial cells (LECs) remain elusive during lymphangiogenesis in tumor hypoxic microenvironment. Recent studies report that loss of SEMA3F critically contributes to lymphangiogenesis of the CRCs. Here, we silenced SEMA3F expression of CRCs and co-culture with hLECs, the tubulogenesis capacity and hLECs migration were escalated in the hypoxia, the hLECs mainly relied on fatty acid metabolism not aerobic glycolysis during lymphangiogenesis. SEMA3F-deficient CRCs up-regulated PMAKP expression and phosphorylation of hLECs, ... More

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